Left ventricular size and function in patients with systemic lupus erythematosus associate with lupus anticoagulant: An echocardiographic follow-up study.

BACKGROUND: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with increased risk of cardiac dysfunction. The pathophysiological mechanisms are poorly understood, and prognostic markers are warranted. PURPOSE: We aimed to identify SLE-characteristics associated with measures of cardiac size and function during a five-year follow-up. METHODS: We included 108 patients with SLE: 90% females, mean age 46 ± 13 years, median disease duration 14 (range 7-21) years. We performed blood sampling for potential biomarkers as well as a standard echocardiography at baseline and at a 5-year follow-up. To investigate associations with baseline and prospective 5-year changes in echocardiographic parameters, we performed multivariate regression analyses of SLE-related baseline variables (clinical disease activity, lupus nephritis, chronic kidney disease, anti-cardiolipin and/or anti-beta-2 glycoprotein I antibodies, and lupus anticoagulant (LAC)) and adjusted for traditional risk factors. RESULTS: During follow-up, diastolic function regressed in two out of five echocardiographic measures (E/A ratio 1.4 ± 0.5 vs. 1.3 ± 0.5, p = 0.002; tricuspid regurgitation peak velocity 2.0 ± 0.6 vs. 2.2 ± 0.4 mmHg, p < 0.001). Left ventricular (LV) end-diastolic volume index increased (43.7 ± 13.9 vs. 52.5 ± 15.7 mL/m2, p < 0.001). Left and right ventricular systolic function remained stationary. LAC was associated with inferior diastolic function: lower E/A ratio (p = 0.04) and higher E/e' ratio at baseline (p = 0.04) and increased left ventricular atrial volume index during follow-up (p = 0.01). LAC was further associated with LV dilatation during follow-up (p = 0.01). CONCLUSION: Presence of LAC was associated with measures of diastolic function as well as progressive LV dilatation during the 5-year follow-up. Thus, LAC might be a predictor of cardiac dysfunction in SLE patients. LAC is known to have implications for the microvascular circulation, but the clinical significance of the present findings is yet to be elucidated.

Myositis-specific autoantibodies and QTc changes by ECG in idiopathic inflammatory myopathies.

OBJECTIVES: The aim of this study was to investigate cardiac involvement detected by ECG in patients with idiopathic inflammatory myopathies (IIMs) and to evaluate possible associations between the autoantibody profile and ECG changes in these patients. METHODS: In a Scandinavian cross-sectional study, patients were included from two Danish centres and one Swedish centre. Resting 12-lead ECG was investigated in 261 patients with IIM compared with 102 patients with systemic sclerosis (SSc) and 48 healthy controls (HCs). ECG changes were correlated to clinical manifestations and myositis-specific and myositis-associated autoantibodies (MSAs and MAAs, respectively). RESULTS: Patients with IIM had a longer mean corrected QT (QTc) duration and more frequently presented with prolonged QTc (≥450 ms; P = 0.038) compared with HCs. A longer QTc duration was recorded in SSc compared with IIM [433 ms (s.d. 23) vs 426 (24); P = 0.011], yet there was no significant difference in the fraction with prolonged QTc (SSc: 22%, IIM: 16%; P = 0.19). In multivariable regression analyses, anti-Mi2 (P = 0.01, P = 0.035) and anti-Pl-7 (P = 0.045, P = 0.014) were associated with QTc duration and prolonged QTc in IIM. Elevated CRP was associated with prolonged QTc (P = 0.041). CONCLUSION: The presence of QTc abnormalities was as common in patients with IIM as in patients with SSc, including prolonged QTc seen in almost one-fifth of the patients. Anti-Mi2, anti-Pl-7 and elevated CRP may serve as biomarkers for cardiac disease in IIM, but needs to be confirmed in a larger prospective study.

Management of Myocarditis in Myositis: Diagnosis and Treatment.

PURPOSE OF REVIEW: To provide a summary of the current knowledge on myocarditis in idiopathic inflammatory myopathies (IIMs). RECENT FINDINGS: There is increasing epidemiological knowledge about heart involvement generally and myocarditis specifically in IIMs. Cardiac magnetic resonance (CMR) plays an important role in this regard. Myocarditis occupies an important place in the spectrum of pathologies that involve the myocardium in patients with IIMs. Nevertheless, its full impact still remains to be elucidated. A larger cooperation between rheumatologists and cardiologists in the clinical, as well as in the research field, is necessary to expand our knowledge in the area.

Beneficial effects of elevating cardiac preload on left-ventricular diastolic function and volume during heat stress: implications toward tolerance during a hemorrhagic insult.

Volume loading normalizes tolerance to a simulated hemorrhagic challenge in heat-stressed individuals, relative to when these individuals are thermoneutral. The mechanism(s) by which this occurs is unknown. This project tested two unique hypotheses; that is, the elevation of central blood volume via volume loading while heat stressed would 1) increase indices of left ventricular diastolic function, and 2) preserve left ventricular end-diastolic volume (LVEDV) during a subsequent simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Indices of left ventricular diastolic function were evaluated in nine subjects during the following conditions: thermoneutral, heat stress, and heat stress after acute volume loading sufficient to return ventricular filling pressures toward thermoneutral levels. LVEDV was also measured in these subjects during the aforementioned conditions prior to and during a simulated hemorrhagic challenge. Heat stress did not change indices of diastolic function. Subsequent volume infusion elevated indices of diastolic function, specifically early diastolic mitral annular tissue velocity (E') and early diastolic propagation velocity (E) relative to both thermoneutral and heat stress conditions (P < 0.05 for both). Heat stress reduced LVEDV (P < 0.05), while volume infusion returned LVEDV to thermoneutral levels. The reduction in LVEDV to LBNP was similar between thermoneutral and heat stress conditions, whereas the reduction after volume infusion was attenuated relative to both conditions (P < 0.05). Absolute LVEDV during LBNP after volume loading was appreciably greater relative to the same level of LBNP during heat stress alone. Thus, rapid volume infusion during heat stress increased indices of left ventricular diastolic function and attenuated the reduction in LVEDV during LBNP, both of which may serve as mechanisms by which volume loading improves tolerance to a combined hyperthermic and hemorrhagic challenge.

Myocardial fibrosis associates with lupus anticoagulant in patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that carries increased risk of cardiovascular disease; however, the underlying pathophysiological mechanisms remain poorly understood. We aimed to investigate the prevalence and degree of myocardial fibrosis in SLE patients and associated disease characteristics. Forty-nine SLE patients (89% female, mean age 52 ± 13 years, median disease duration 19 (11-25) years) and 79 sex-and age-matched healthy controls were included. CMR with T1 mapping was performed on SLE patients and healthy controls. Fifty-one SLE patients received gadolinium contrast for the evaluation of late gadolinium enhancement (LGE) and extra cellular volume (ECV). Multiple linear regression analyses were performed to investigate the association between markers of myocardial fibrosis on CMR (LGE, T1, ECV) and SLE-related variables [clinical disease activity, lupus nephritis, chronic kidney disease, anti-cardiolipin and/or anti-beta-2 glycoprotein I antibodies, and lupus anticoagulant (LAC)] with adjustment for traditional risk factors. T1 values were elevated in SLE patients compared to healthy controls (1031 ± 36 ms vs. 1019 ± 25 ms, p = 0.01). LGE was present in 20% of SLE patients who received gadolinium contrast. On multivariable analysis, LAC was associated with LGE in SLE patients (ß = 3.87, p = 0.02). Neither T1 nor ECV associated with SLE disease characteristics; however, there was a trend towards an association between LAC and T1 (ß = 16.9, p = 0.08). SLE patients displayed signs of myocardial fibrosis on CMR that were associated with the presence of LAC. These findings support the pathophysiological understanding of LAC as a mediator of microvascular and subsequent myocardial dysfunction.

Sex-and age-related variations in myocardial tissue composition of the healthy heart: a native T1 mapping cohort study.

AIMS: Cardiovascular diseases manifest differently in males and females, potentially influenced by inherent sex- and age-related differences in myocardial tissue composition. Such inherent differences are not well-established in the literature. With this study using cardiac magnetic resonance (CMR) native T1 mapping, we aim to determine the effect of sex and age on myocardial tissue composition in healthy individuals. METHODS AND RESULTS: CMR native T1 mapping was performed in 276 healthy individuals (55% male, age 8---84 years) on a 1.5 Tesla scanner using a MOLLI 5(3)3 acquisition scheme. Additionally, 30 healthy participants (47% male, age 24-68 years) underwent a 1-year follow-up CMR to assess the longitudinal changes of native T1. Mean native T1 values were 1000 ± 22 ms in males and 1022 ± 23 ms in females [mean difference (MD) = 22 ms, 95% confidence interval (CI) (17, 27)]. Female sex was associated with higher native T1 in multivariable linear regression adjusting for age, heart rate, left ventricular mass index, and blood T1 [ß=10 ms, 95% CI (3.4, 15.8)]. There was no significant interaction between sex and age (P = 0.27). Further, age was not associated with native T1 [ß=0.1 ms, 95% CI (-0.02, 0.2)], and native T1 did not change during a 1-year period [MD -4 ms, 95% CI (-11, 3)]. CONCLUSION: Female sex was associated with higher native T1; however, there was no association between age and native T1. Additionally, there was no evidence of an interaction between sex and age. Our findings indicate intrinsic sex-based disparities in myocardial tissue composition.

The COVID-19 in athletes (COVA) study: a national study on cardio-pulmonary involvement of SARS-CoV-2 infection among elite athletes.

Background: COVID-19 can cause cardiopulmonary involvement. Physical activity and cardiac complications can worsen prognosis, while pulmonary complications can reduce performance. Aims: To determine the prevalence and clinical implications of SARS-CoV-2 cardiopulmonary involvement in elite athletes. Methods: An observational study between 1 July 2020 and 30 June 2021 with the assessment of coronary biomarkers, electrocardiogram, echocardiography, Holter-monitoring, spirometry, and chest X-ray in Danish elite athletes showed that PCR-tested positive for SARS-CoV-2. The cohort consisted of male football players screened weekly (cohort I) and elite athletes on an international level only tested if they had symptoms, were near-contact, or participated in international competitions (cohort II). All athletes were categorized into two groups based on symptoms and duration of COVID-19: Group 1 had no cardiopulmonary symptoms and duration ≤7 days, and; Group 2 had cardiopulmonary symptoms or disease duration >7 days. Results: In total 121 athletes who tested positive for SARS-CoV-2 were investigated. Cardiac involvement was identified in 2/121 (2%) and pulmonary involvement in 15/121 (12%) participants. In group 1, 87 (72%), no athletes presented with signs of cardiac involvement, and 8 (7%) were diagnosed with radiological COVID-19-related findings or obstructive lung function. In group 2, 34 (28%), two had myocarditis (6%), and 8 (24%) were diagnosed with radiological COVID-19-related findings or obstructive lung function. Conclusions: These clinically-driven data show no signs of cardiac involvement among athletes who tested positive for SARS-CoV-2 infection without cardiopulmonary symptoms and duration <7 days. Athletes with cardiopulmonary symptoms or prolonged duration of COVID-19 display, exercise-limiting cardiopulmonary involvement.

[Paradox embolism in a patient with pulmonary embolism and unknown patent foramen ovale].

This case report describes a 64-year-old male patient, who presented with sudden onset dyspnoea. A chest CT-angiography revealed the presence of central bilateral pulmonary embolisms (PE), and he was admitted for anticoagulative treatment. Shortly after admission, he developed discomfort and pulselessness in the right leg, and a limb CT-angiography revealed a femoral artery thrombus. PE in conjunction with acute limb ischaemia raised suspicion of a paradoxical mechanism of systemic embolism, which was confirmed by echocardiography with thrombus straddling a patent foramen ovale.

Cardiac arrest in anti-mitochondrial antibody associated inflammatory myopathy.

Insight into predictors of cardiac involvement in inflammatory myopathies is sparse. A negative prognostic role of anti-mitochondrial antibodies (AMA) has been noticed and is supported by the current case. We describe a male patient who at the age 40 suffered a cardiac arrest and over the following months experienced progressive heart failure, arrhythmias and proximal muscle weakness. Clinical, genetic and serologic testing and repeated imaging- and histopathological investigations resulted in a diagnosis of AMA-associated, necrotizing, inflammatory myositis with cardiac involvement. Besides a cardiac resynchronization therapy defibrillator, heart failure and antiarrhythmic drugs the patient received successive immunosuppressants, which improved skeletal muscle strength but not cardiac disease progression. At age 45 he died from end-stage heart failure. Clinicians must be aware of AMA-associated myositis as a cause of unclarified heart disease, even in patients with initially sparse extra-cardiac manifestations. Further knowledge of treatment strategies is highly needed for this disease entity.

Hereditary hemochromatosis (HFE) genotypes in heart failure: relation to etiology and prognosis.

BACKGROUND: It is believed that hereditary hemochromatosis (HH) might play a role in cardiac disease (heart failure (HF) and ischemia). Mutations within several genes are HH-associated, the most common being the HFE gene. In a large cohort of HF patients, we sought to determine the etiological role and the prognostic significance of HFE genotypes. METHODS: We studied 667 HF patients (72.7% men) with depressed systolic function, enrolled in a multicentre trial with a follow-up period of up to 5 years. All were genotyped for the known HFE variants C282Y, H63D and S65C. RESULTS: The genotype and allele frequencies in the HF group were similar to the frequencies determined in the general Danish population. In multivariable analysis mortality was not predicted by C282Y-carrier status (HR 1.2, 95% CI: 0.8-1.7); H63D-carrier status (HR 1.0, 95% CI: 0.7-1.3); nor S65C-carrier status (HR 1.2, 95% CI: 0.7-2.0). We identified 27 (4.1%) homozygous or compound heterozygous carriers of HFE variants. None of these carriers had a clinical presentation suggesting hemochromatosis, but hemoglobin and ferritin levels were higher than in the rest of the cohort. Furthermore, a trend towards reduced mortality was seen in this group in univariate analyses (HR 0.4, 95% CI: 0.2-0.9, p = 0.03), but not in multivariate (HR 0.5, 95% CI: 0.2-1.2). CONCLUSION: HFE genotypes do not seem to be a significant contributor to the etiology of heart failure in Denmark. HFE variants do not affect mortality in HF.

The prevalence and relevance of the Brugada-type electrocardiogram in the Danish general population: data from the Copenhagen City Heart Study.

AIMS: The prevalence of the Brugada-type electrocardiogram (ECG) in the Danish population is not known. METHODS AND RESULTS: Inhabitants from the city of Copenhagen, Denmark, have participated in a prospective study since 1976. Four cross-sectional surveys have been carried out. Follow-up was performed using public registers. At each examination, the participants had an ECG registered. ECGs, showing right bundle branch block (RBBB) were examined for a possible Brugada-type pattern. A total of 42,560 ECGs had been registered from 18,974 participants. 1,284 had been coded as RBBB. Among these ECGs, we found no ECGs showing type 1 Brugada pattern, and 14 showing type 2 or 3 pattern. The prevalence of the total number of ECGs with Brugada pattern was 7/10,000. None of the subjects with a Brugada-pattern ECG died suddenly during follow-up. CONCLUSION: The Brugada-type ECG pattern is rare in the general Danish population. None of the subjects with a Brugada-type ECG died suddenly during a follow-up of 6-33 years.

Predictors of exercise capacity and symptoms in severe aortic stenosis.

AIMS: This study investigated the association between invasive and non-invasive estimates of left ventricular (LV) filling pressure and exercise capacity, in order to find new potential candidates for risk markers in severe aortic valve stenosis (AS). METHODS AND RESULTS: Twenty-nine patients with AS, aortic valve area (AVA) < 1 cm(2), performed a symptom-limited multistage supine bicycle exercise test. Immediately before the exercise test, the pulmonary capillary wedge pressure (PCWP), Doppler index for LV filling (E/e'), and left atrial (LA) volume were measured. Symptomatic status was determined by senior staff doctors blinded to the results of this study. All patients terminated the exercise test because of dyspnoea. There were no significant differences in AVA between asymptomatic patients (n = 9) and symptomatic patients (n = 20), and AVA did not correlate with exercise capacity (r = -0.16, P = NS). In contrast, PCWP, LA volume, and E/e' were significantly increased in the symptomatic group and they all correlated with exercise capacity (r = -0.66, -0.75, and -0.62, respectively, P < 0.001). Receiver operating characteristic curve analysis confirmed that PCWP, LA volume index, and E/e' all provided incremental information [area under the curve (AUC) = 0.90, 0.92, and 0.90, respectively, P < 0.05] over AVA index (AUC = 0.66, NS) in predicting symptomatic status. CONCLUSION: PCWP, LA volume, or E/e' is closely related to exercise capacity and symptomatic status, and may therefore be important markers of disease severity in AS. Clinical Trials.gov Identifier: NCT00252317 (http://clinicaltrials.gov/ct2/results?term=NCT00252317).

Comparison of Valsalva manoeuvre and exercise in echocardiographic evaluation of left ventricular outflow tract obstruction in hypertrophic cardiomyopathy.

AIMS: Several methods are used to induce latent left ventricular outflow tract (LVOT) gradients in patients with hypertrophic cardiomyopathy (HCM). We compared LVOT gradients induced by Valsalva manoeuvre (VM) and exercise echocardiography (EE) in patients with HCM treated with percutaneous transluminal septal myocardial ablation (PTSMA). METHODS AND RESULTS: Left ventricular outflow tract gradients were measured at rest, during VM, and during EE in 57 patients 3.8 ± 2.8 years after PTSMA. Measurement succeeded in all patients during VM and in 96% during EE. There were no differences in LVOT gradients between VM [17 (9-33) mmHg] and EE [18 (10-30) mmHg, P = 0.31] [median (inter-quartile range)], but the differences ranged from -45 to 84 mmHg in individual patients. In 93% of patients, EE had no influence on the categorization into manifest-, latent- or non-obstructive phenotypes. The 7%, who revealed LVOT gradients ≥30 mmHg only during EE, did not reach LVOT gradients of 50 mmHg. Patients improving two New York Heart Association (NYHA) classes after PTSMA had higher baseline LVOT gradients during VM [115 (72-160) vs. 88 (54-114) mmHg, P = 0.04] and a larger reduction in VM-induced LVOT gradients [80 (48-139) vs. 61 (28-83) mmHg, P = 0.02] than patients improving one NYHA class. CONCLUSION: Valsalva manoeuvre and EE induce similar degrees of LVOT gradient, but categorization into obstructive phenotypes was not influenced by EE in more than 90% of patients. Valsalva manoeuvre should be the primary choice of stress modality in HCM patients treated with PTSMA, but EE is essential for the clinical management of the entire cohort.

Long-term impact of diabetes in patients hospitalized with ischemic and non-ischemic heart failure.

OBJECTIVES: Diabetes mellitus (DM) in combination with heart failure (HF) is associated with a high risk of death, but it is uncertain whether the prognosis differs in ischemic and non-ischemic HF groups. DESIGN: One thousand, three hundred and six patients with ischemic HF and 1315 patients with non-ischemic HF were followed for 6.8 years. Risk of all caue mortality was analyzed using Cox proportional hazard models. RESULTS: Mean age was 73 (+/- standard deviation 11) years. Two hundred and forty eight of 1306 (19%) patients with ischemic HF and 172/1315 (13%) patients with non-ischemic HF had DM (p for difference < 0.0001). Overall, 939/1306 (72%) patients in the ischemic HF group, and 835/1315 (64%) patients in the non-ischemic HF group died, respectively. Totally 191/248 (77%) DM patients with ischemic HF, and 127/172 (74%) DM patients with non-ischemic HF died. DM was associated with adjusted hazard ratios (HR) of 1.45 (1.22-1.73, p < 0.0001) if ischemic HF, and 1.50 (1.22-1.84, p < 0.0001) if non-ischemic HF (p for interaction = 0.4), compared to non-DM non-ischemic HF patients. CONCLUSION: The long-term prognosis of DM is equally adverse in ischemic and non-ischemic HF patients.

Determinants of exercise-induced increase of mitral regurgitation in patients with acute coronary syndromes.

BACKGROUND: Mechanisms behind exercise-induced increase of mitral regurgitation (MR) in patients with chronic ischemic heart disease have been described earlier. We describe the determinants of exercise-induced changes in MR in patients with non-ST-elevation acute coronary syndrome (NSTACS). METHODS: Forty-five consecutive patients (mean + or - SD age 64 + or - 10 years, 37 men) with NSTACS underwent exercise echocardiography on a supine bicycle the day before angiography. The exercise was started with a load of 10 W with increments of 10 W every minute until symptoms developed or a max load of 100 W. Effective regurgitation orifice (ERO) was measured at rest and at peak exercise. RESULTS: Twelve patients had more than trace MR at rest with ERO 8 + or - 5 (mean + or - SD), range: 3-18 mm(2). In these patients, ERO increased during exercise to 13 + or - 6 (mean + or - SD), range: 6-23 mm(2) corresponding to an increase of 70% from rest (P = 0.001). Seven other patients developed new MR during exercise with ERO at peak exercise of 8 + or - 4 mm(2) (mean + or - SD), range: 4-14 mm(2). All these patients had significant increase in wall motion score index (WMSI) of 0.14 + or - 0.18 (mean + or - SD), P = 0.006, while in the 25 patients without MR at rest or during exercise, WMSI remained unchanged, -0.02 + or - 0.08 (mean + or - SD), P = 0.2. CONCLUSION: Exercise-induced increases of MR in patients with NSTACS are related to worsening of regional wall motions. (Echocardiography 2010;27:567-574).

Moderate exercise does not increase the severity of mitral regurgitation due to mitral valve prolapse.

BACKGROUND: Mitral regurgitation (MR) secondary to ischemic heart disease (IHD) increases during exercise. We tested the hypothesis that the same is also true for MR due to mitral valve prolapse (MVP). METHODS: Consecutive patients with asymptomatic MR of varying severity underwent exercise test on a supine bicycle with workload up to a maximum of 100 W. Echocardiographic measurements were performed at rest and at peak exercise. The study was designed to detect an effective regurgitant orifice (ERO) change of at least 10 mm² during exercise. RESULTS: Twenty-six patients (21 male, age 56 ± 12 years (mean ± SD)) were included. Patients had an ERO of 35 ± 23 mm² (mean ± SD) and regurgitation volume of 48 ± 38 mL (mean ± SD). In these patients, ERO remained unchanged (an increase of 2 ± 15 mm² during exercise, P = 0.6). The regurgitation volume (RVol) decreased with 11 ± 16 mL (mean ± SD), P = 0.003. When calculated for 1 minute, RVol increased during exercise (P = 0.01), but in relation to the total cardiac output it decreased significantly (P = 0.02). CONCLUSION: Exercise does not increase the severity of MR due to MVP, in contrast to MR secondary to IHD. Different disease mechanisms behind these two types of MR could explain this difference.

[Randomised double-blind tests and invasive cardiology].

Virtually all the new medical treatments nowadays are tested in randomised double-blind tests, before they are introduced as routine treatment. However, this is not always the case for the new surgical or catheter-based treatments. Although different in some aspects, it is practically possible for surgical and catheter-based treatments to follow the same scientific principles as medical treatments in order to test their efficacy. In this review, we argue that it is necessary to conduct randomised double-blind tests of these interventions prior to their introduction in clinical practice.

Postoperative atrial fibrillation after aortic valve replacement is a risk factor for long-term atrial fibrillation.

OBJECTIVES: Postoperative atrial fibrillation (POAF) is a common complication following cardiac surgery. However, knowledge on the rate of long-term atrial fibrillation (LTAF) after POAF remains unclear. We investigated predictors of POAF in patients with aortic stenosis undergoing surgical aortic valve replacement, and assessed the rate of LTAF during follow-up. METHODS: We prospectively included 96 adult patients with severe aortic stenosis undergoing surgical aortic valve replacement. Patients with previous atrial fibrillation (AF) were excluded. Patients underwent echocardiography, cardiac computed tomography and magnetic resonance imaging immediately prior to surgery. Surgical aortic clamp time and postoperative C-reactive protein (CRP) were documented. POAF was defined as AF recorded within 7 days of surgery. Through chart review, patients were followed up for documented episodes of LTAF occurring more than 7 days after surgery. RESULTS: POAF occurred in 51 patients (53%). It was associated with larger preoperative echocardiographic left atrial volume index (44 ± 12 vs 37 ± 8 ml/m2, P = 0.004), longer aortic clamp time [80 (70-102) vs 72 (62-65) min, P = 0.04] and higher CRP on first postoperative day [80 (64-87) vs 65 (44-83) mg/l, P = 0.001]. Multivariable logistic regression revealed that left atrial volume index [odds ratio (OR) 1.07, 95% confidence interval (CI) 1.02-1.13; P = 0.005] and postoperative CRP (OR 1.03, 95% CI 1.01-1.05; P = 0.006) were the only independent predictors of POAF. During 695 days (25th-75th percentile: 498-859 days) of follow-up, LTAF occurred in 11 patients of whom 10 were in the POAF group (hazard ratio 9.4, 95% CI 1.2-74; P = 0.03). CONCLUSIONS: POAF is predicted by left atrial volume index and postoperative CRP. Patients with POAF have a 9-fold increase risk of developing symptomatic LTAF during follow-up. CLINICAL TRIAL REGISTRATION NUMBER: ClinicalTrials.gov (NCT02316587).

Association between left ventricular diastolic function and right ventricular function and morphology in asymptomatic aortic stenosis.

BACKGROUND: Aortic stenosis (AS) is a progressive disease in which left ventricular (LV) diastolic dysfunction is common. However, the association between diastolic dysfunction and right ventricular (RV) loading conditions and function has not been investigated in asymptomatic AS patients. METHODS AND FINDINGS: A total of 41 patients underwent right heart catheterization and simultaneous echocardiography at rest and during maximal supine exercise, stratified according to resting diastolic function. Cardiac chamber size and morphology was assessed using cardiac magnetic resonance imaging (cMRI). RV stroke work index, pulmonary artery (PA) compliance, PA elastance, PA pulsatility index, and right atrial pressure (RAP) were calculated at rest and maximal exercise. Ten patients (24%) had normal LV filling pattern, 20 patients (49%) had grade 1, and 11 patients (27%) had grade 2 diastolic dysfunction. Compared to patients with normal diastolic filling pattern, patients with diastolic dysfunction had lower RV end-diastolic volume (66 ± 11 ml/m2 vs. 79 ± 15 ml/m2, p = 0.02) and end-systolic volume (25 ± 7 ml/m2 vs. 32 ± 9 ml/m2, p = 0.04). An increase in mean RAP to ≥15 mmHg following exercise was not seen in patients with normal LV filling, compared to 4 patients (20%) with mild and 7 patients (63%) with moderate diastolic dysfunction (p = 0.003). PA pressure and PA elastance was increased in grade 2 diastolic dysfunction and correlated with RV volume and maximal oxygen consumption (r = -0.71, p < 0.001). CONCLUSIONS: Moderate diastolic dysfunction is associated with increased RV afterload (elastance), which is compensated at rest, but is associated with increased RAP and inversely related to maximal oxygen consumption during maximal exercise.

End-systolic wall stress in aortic stenosis: comparing symptomatic and asymptomatic patients.

Aims: In aortic stenosis (AS), there is poor association between symptoms and conventional markers of AS severity or left ventricular (LV) systolic function. This may reflect that symptoms arise from LV diastolic dysfunction or that aortic valve area (AVA) and transvalvular gradient do not reflect afterload. We aimed to study the impact of afterload (end-systolic wall stress [ESWS]) on the presence of symptoms in AS and to test whether symptoms are related to increased ESWS or LV remodelling. Methods and results: In a prospective study, ESWS was estimated by measuring LV wall thickness from MRI and estimated LV end systolic pressure from echocardiographic mean gradient and systolic blood pressure in 78 patients with severe AS scheduled for aortic valve replacement and 91 patients with asymptomatic severe AS. Symptomatic patients had lower indexed AVA (0.40±0.11 vs 0.45±0.09 cm2/m2, p=0.009). They had undergone more extensive remodelling (MRI LV mass index [LVMi]: 85±24 vs 69±17 g/m2, p<0.0001), had higher tricuspid regurgitant gradient (24±8 mm Hg vs 19 ± 7 mm Hg, p=0.0001) and poorer global longitudinal strain (-15.6±3.8 vs -19.9±3.2%, p<0.0001). ESWS was higher among symptomatic patients (96±51 vs 76±25 kdynes/cm2, p=0.003). Multivariate logistic regression identified echocardiographic relative wall thickness, tricuspid gradient, mitral deceleration time, early diastolic strain rate, MRI LVMi, MRI LV end-diastolic volume index and ESWS as independently associated with being symptomatic. Conclusion: ESWS can be estimated from multimodality imaging combining MRI and echocardiography. It is correlated with LV remodelling and neurohormonal activation and is independently associated with symptomatic status in AS.